Evidence map›Paper›PMID 21127830›Full record

SynthesisDiabetologia2011

Genetic associations in diabetic nephropathy: a meta-analysis.

A L Mooyaart, E J J Valk, L A van Es, J A Bruijn, E de Heer, B I Freedman, O M Dekkers, H J Baelde

Erratum issuedAbstract readMeta-Analysis
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Diabetologia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 117 papers, 12 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed, 12 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

117 citing papers in PubMed, 12 syntheses or guidelines pooled it.

  1. The Role ofGenes · 2025
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  18. Correlation between polymorphisms ofZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
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  20. Article

57 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors.

A L MooyaartDepartment of Pathology, Bldg.1, L1-Q, Leiden University Medical Center, PO Box 9600, 2300 RC, Leiden, the Netherlands. a.l.mooyaart@lumc.nl
E J J Valk
L A van Es
J A Bruijn
E de Heer
B I Freedman
O M Dekkers
H J Baelde

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisThis meta-analysis assessed the pooled effect of each genetic variant reproducibly associated with diabetic nephropathy.

methodsPubMed, EMBASE and Web of Science were searched for articles assessing the association between genes and diabetic nephropathy. All genetic variants statistically associated with diabetic nephropathy in an initial study, then independently reproduced in at least one additional study, were selected. Subsequently, all studies assessing these variants were included. The association between these variants and diabetic nephropathy (defined as macroalbuminuria/proteinuria or end-stage renal disease [ESRD]) was calculated at the allele level and the main measure of effect was a pooled odds ratio. Pre-specified subgroup analyses were performed, stratifying for type 1/type 2 diabetes mellitus, proteinuria/ESRD and ethnic group.

resultsThe literature search yielded 3,455 citations, of which 671 were genetic association studies investigating diabetic nephropathy. We identified 34 replicated genetic variants. Of these, 21 remained significantly associated with diabetic nephropathy in a random-effects meta-analysis. These variants were in or near the following genes: ACE, AKR1B1 (two variants), APOC1, APOE, EPO, NOS3 (two variants), HSPG2, VEGFA, FRMD3 (two variants), CARS (two variants), UNC13B, CPVL and CHN2, and GREM1, plus four variants not near genes. The odds ratios of associated genetic variants ranged from 0.48 to 1.70. Additional variants were detected in subgroup analyses: ELMO1 (Asians), CCR5 (Asians) and CNDP1 (type 2 diabetes). CONCLUSIONS/

interpretationThis meta-analysis found 24 genetic variants associated with diabetic nephropathy. The relative contribution and relevance of the identified genes in the pathogenesis of diabetic nephropathy should be the focus of future studies.

Indexed as

Adaptor Proteins, Signal TransducingApolipoprotein C-IApolipoproteins ECarboxypeptidasesDiabetic NephropathiesDipeptidasesErythropoietinGenetic VariationHeparan Sulfate ProteoglycansHumansIntercellular Signaling Peptides and ProteinsNerve Tissue ProteinsNitric Oxide Synthase Type IIIPeptidyl-Dipeptidase APolymorphism, GeneticReceptors, CCR5ACE protein, humanAdaptor Proteins, Signal TransducingAPOC1 protein, humanApolipoprotein C-IApolipoproteins ECarboxypeptidasesCNDP1 protein, humanCPVL protein, humanDipeptidasesELMO1 protein, humanEPO protein, humanErythropoietinGREM1 protein, humanHeparan Sulfate ProteoglycansIntercellular Signaling Peptides and ProteinsNerve Tissue ProteinsNitric Oxide Synthase Type IIINOS3 protein, humanPeptidyl-Dipeptidase AperlecanReceptors, CCR5UNC13B protein, human

Identifiers

PMID21127830
PMCPMC3034040

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Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.